Hypertrophic Obstructive Cardiomyopathy: Septal Ablation With Overlapping Sirolimus-Eluting and Covered Stents After Failed Alcoholization and Concomitant Coronary Artery Disease

A 61-year-old man with exertional dyspnea was diagnosed with hypertrophic obstructive cardiomyopathy. The echocardiogram demonstrated an interventricular septum with a thickness of 18 mm, marked systolic anterior motion, and mitral regurgitation grade 3. The left ventricular outflow tract (LVOT) gradient was 100 mm Hg. The patient was treated with percutaneous transluminal septal myocardial alcohol ablation, resulting in a residual LVOT gradient of 20 mm Hg. Mild coronary artery disease of the proximal left anterior descending coronary artery (LAD) and the first diagonal branch (D1) (40% diameter stenosis by quantitative coronary angiography) was left untreated.

The patient remained asymptomatic for 6 months and then again had development of exertional dyspnea. The echocardiogram revealed relapse of the LVOT gradient (80 mm Hg). Repeat percutaneous transluminal septal myocardial alcohol ablation was planned. The invasive LVOT gradient was 77 mm Hg. Coronary angiography demonstrated progression of the disease of both lesions in the LAD and D1 (70% by quantitative coronary angiography). Because of the concomitant coronary artery disease, the treatment plan was changed. The LAD and the D1 were treated with sirolimus-eluting stent implantation (Figure 1A). Instead of injecting ethanol, a polytetrafluoroethylene-covered stent was implanted within the borders of the sirolimus-eluting stent over the ostium of the septal artery (Figure 1B). The procedure resulted in occlusion of the septal branch and immediate reduction of the LVOT gradient to 12 mm Hg (Figure 1C). The creatine kinase level rose to 789 IU/L. At 12 months’ follow-up, the patient remained asymptomatic. Repeat angiography revealed no restenosis (Figure 1D), and intravascular ultrasound showed complete absence of neointima formation (Figure 1F and 1G). Furthermore, no signs of septal collateralization through the right coronary artery were noted (Figure 1E). There was no rest gradient. Multislice computed tomography imaging demonstrated good stent patency (Figure 2), and magnetic resonance imaging with gadolinium demonstrated the region of the infarcted interventricular septum (Figure 3). Septal reperfusion through collaterals leading to treatment failure after occlusion with covered stents has been previously reported.^1,2 In our case, this probably was prevented by myocardial fibrosis and destruction of the microcirculation after the initial alcoholization.